Multicentric Hospital-Based Surveillance of Pertussis Amongst Infants Admitted in Tertiary Care Facilities in India.

OBJECTIVE: To estimate the disease and economic burden of pertussis amongst hospitalised infants in India. DESIGN: Multicentric hospital-based surveillance study. PARTICIPANTS: Hospitalised infants with clinical suspicion of pertussis based on predefined criteria. OUTCOME MEASURES: Proportion of infants with laboratory-confirmed pertussis, economic burden of pertussis amongst hospitalised infants. RESULTS: 693 clinically suspected infants were recruited of which 32 (4.62%) infants had laboratory-confirmed pertussis. Progressive cough with post-tussive emesis (50%) and pneumonia (34%) were the common clinical presentations; apnea in young infants was significantly associated with pertussis. Infants with pertussis were more likely to be younger (median age 102.5 days vs.157 days) and born preterm (42.9% vs 24.5%). Almost 30% infants with pertussis had not received vaccine for pertussis with 50% of these infants aged less than 2 months. Pertussis was associated with higher costs of hospitalisation, pharmacy and loss of working days by caregivers as compared to non-pertussis cases. CONCLUSIONS: Younger infants, those born preterm and those inadequately immunised against pertussis are at higher risk of pertussis infection. Timely childhood immunisation and introduction of maternal immunisation for pertussis can help in reducing the disease burden.

Susceptibility to mouse cytomegalovirus is associated with deletion of an activating natural killer cell receptor of the C-type lectin superfamily.

Cytomegalovirus is the leading cause of congenital viral disease and the most important opportunistic infection in immunocompromised patients. We have used a mouse experimental infection model (MCMV) to study the genetic parameters of host/virus interaction. Susceptibility to infection with MCMV is controlled by Cmv1, a chromosome 6 locus that regulates natural killer (NK) cell activity against virally infected targets. Here, we use a positional cloning strategy to isolate the gene mutated at the Cmv1 locus. Cmv1 maps within a 0.35-cM interval defined by markers D6Ott8 and D6Ott115, which corresponds to a physical distance of 1.6 Mb (refs. 6-8). A transcript map of the region identified 19 genes, including members of the killer cell lectin-like receptor family a (Klra, formerly Ly49; refs. 9-12), which encode inhibitory or activating NK cell receptors that interact with MHC class I molecules. Klra genes have different copy numbers and genomic organization, and are highly polymorphic among inbred strains, making it difficult to distinguish between normal allelic variants and distinct Klra genes, or possible mutations associated with Cmv1. The recombinant inbred strain BXD-8/Ty (BXD-8; ref. 18), derived from Cmv1r C57BL/6 (B6, resistant) and Cmv1s DBA/2 (susceptible), is of particular interest because it is highly susceptible to MCMV infection despite having a B6 haplotype at Cmv1. We determined that MCMV susceptibility in BXD-8 is associated with the deletion of Klra8 (formerly Ly49h).